Methods and apparatus for reducing localized circulatory system pressure

ABSTRACT

The present invention is directed to methods and apparatus for decreasing pressure in the left atrium of a patient by implanting a valved shunt through the atrial septum, whereby a volume of blood sufficient to reduce pressure in said left atrium is released to the right atrium.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application is a continuation under 35 U.S.C. §120 of U.S. patentapplication Ser. No. 09/839,643, filed Apr. 20, 2001 now U.S. Pat. No.8,091,556 and entitled “Methods and Apparatus for Reducing LocalizedCirculatory System Pressure,” the entire contents of which areincorporated herein by reference.

FIELD OF THE INVENTION

The present invention relates to treatments for reducing specificlocalized points of high pressure within the circulatory system, andmore particularly to methods and apparatus to either acutely orchronically reduce left ventricular diastolic pressure that is createdas a result of congestive heart failure or similar indications.

BACKGROUND OF THE INVENTION

Congestive heart failure (CHF) is recognized as the most common cause ofhospitalization and mortality in Western society. CHF is an extremelyserious affliction that has a great impact on the quality of life; itinvolves the loss of heart rate variability and rate responsivemechanisms in the heart, leading to impaired ventricular relaxation andlow exercise tolerance. The disease afflicts about 4 million Americansin any given year; in the USA alone, there are annually about 400,000new cases, 1 million hospital admissions, and $8 billion cost of care.Congestive heart failure is a syndrome characterized by left ventriculardysfunction, reduced exercise tolerance, impaired quality of life anddramatically shortened life expectancy. Decreased contractility of theleft ventricle leads to reduced cardiac output with consequent systemicarterial and venous vasoconstriction. CHF develops generally in thecourse of months or years, and can be the end stage of chronichypertension, infarction, angina, or diabetes. Heart failure, howevercaused, represents an intrinsic property of the muscle, and slowrelaxation due to slow intracellular calcium removal by the sarcoplasmicreticulum is an important factor. In the normal, healthy heart theduration of contraction and relaxation decreases with increasing heartrate. This ensures a diastolic period of sufficient duration, which isimportant (a) for filling of the ventricle, and (b) because coronaryperfusion and myocardial oxygen supply occurs only during diastole. Theduration of contraction and relaxation is determined by calcium removalfrom the contractile filaments, mainly by the calcium pump in thesarcoplasmic reticulum Increased heart rate causes more rapid relaxationdue to increased activation of the calcium pump. The latter mechanism isimpaired in the hypertrophied or failing heart due to reducedtranscription of the genes that supply the calcium pump proteins.Therefore, in heart failure patients an increase of heart rate mayalmost abolish the diastolic interval, which leads to reducedventricular filling, and reduces myocardial blood supply (Davies et al.,1995, “Reduced Contraction and Altered Frequency Response of IsolatedVentricular Myocytes From Patients With Heart Failure,” Circulation 92:2540-2549).

The syndrome of heart failure is a common course for the progression ofmany forms of heart disease. Heart failure may be considered to be thecondition in which an abnormality of cardiac function is responsible forthe inability of the heart to pump blood at a rate commensurate with therequirements of the metabolizing tissues, or can do so only at anabnormally elevated filling pressure. There are many specific diseaseprocesses that can lead to heart failure with a resulting difference inpathophysiology of the failing heart, such as the dilatation of the leftventricular chamber. Etiologies that can lead to this form of failureinclude idiopathic cardiomyopathy, viral cardiomyopathy, and ischemiccardiomyopathy. The process of ventricular dilatation is generally theresult of chronic volume overload or specific damage to the myocardiumIn a normal heart that is exposed to long term increased cardiac outputrequirements, for example, that of an athlete, there is an adaptiveprocess of ventricular dilation and myocyte hypertrophy. In this way,the heart fully compensates for the increased cardiac outputrequirements. With damage to the myocardium or chronic volume overload,however, there are increased requirements put on the contractingmyocardium to such a level that this compensated state is never achievedand the heart continues to dilate. The basic problem with a largedilated left ventricle is that there is a significant increase in walltension and/or stress both during diastolic filling and during systoliccontraction. In a normal heart, the adaptation of muscle hypertrophy(thickening) and ventricular dilatation maintain a fairly constant walltension for systolic contraction. However, in a failing heart, theongoing dilatation is greater than the hypertrophy and the result is arising wall tension requirement for systolic contraction. This is feltto be an ongoing insult to the muscle myocyte resulting in furthermuscle damage. The increase in wall stress is also true for diastolicfilling. Additionally, because of the lack of cardiac output, there isgenerally a rise in ventricular filing pressure from several physiologicmechanisms. Moreover, in diastole there is both a diameter increase anda pressure increase over normal, both contributing to higher wall stresslevels. The increase in diastolic wall stress is felt to be the primarycontributor to ongoing dilatation of the chamber.

Presently available treatments for CHF fall into three generallycategories: (1) pharmacological, e.g., diuretics; (2) assist systems,e.g., pumps; and (3) surgical treatments. With respect topharmacological treatments, diuretics have been used to reduce theworkload of the heart by reducing blood volume and preload. While drugtreatment improves quality of life, it has little effect on survival.Current pharmacological treatment includes a combination of diuretics,vasodilators, inotropes, .beta.-blockers, andAngiotensin-Converting-Enzy-me (ACE)-inhibitors (Bristow & Gilbert,1995, “Improvement in Cardiac Myocyte Function by Biological Effects ofMedical Therapy: A New Concept in the Treatment of Heart Failure,”European Heart Journal 16, Supplement F: 20-31). The effect is adecrease of symptoms, and improved quality of life, but little change inmortality. Moreover, the exercise tolerance of most patients isextremely low, as a consequence of limited oxygen supply through thelungs. Long lasting lack of exercise and malnutrition may contribute tothe condition and partly explain the exercise intolerance. Indeed, thelack of exercise and deterioration of cardiac muscle may each contributeto each other, with a snowballing effect (Coats et al., 1992,“Controlled Trial of Physical Training in Chronic Heart Failure:Exercise Performance, Hemodynamics, Ventilation, and AutonomicFunction,” Circulation 85: 2119-2131). Clinically, preload is defined inseveral ways including left ventricular end diastolic pressure (LVEDP),or left ventricular end diastolic volume (LVEDV). Physiologically, thepreferred definition is the length of stretch of the sarcomere at enddiastole. Diuretics reduce extra cellular fluid that builds incongestive heart failure patients increasing preload conditions.Nitrates, arteriolar vasodilators, angiotensin converting enzymeinhibitors have been used to treat heart failure through the reductionof cardiac workload through the reduction of afterload. Afterload may bedefined as the tension or stress required in the wall of the ventricleduring ejection. Inotropes such as digoxin are cardiac glycosides andfunction to increase cardiac output by increasing the force and speed ofcardiac muscle contraction. These drug therapies offer some beneficialeffects but do not stop the progression of the disease. Captopril,enalapril and other inhibitors of angiotensin-converting enzyme (ACE)have been used to treat congestive heart failure. See Merck Index, 1759and 3521(11th ed. 1989); Kramer, B. L. et al. Circulation 1983,67(4):755-763. However, such ACE inhibitors have generally provided onlymoderate or poor results. For example, captopril therapy generallyprovides only small increases in exercise time and functional capacity.Captopril also has provided only small reductions in mortality rates.

Assist devices used to treat CHF include, for example, mechanical pumps.Mechanical pumps reduce the load on the heart by performing all or partof the pumping function normally done by the heart. Currently,mechanical pumps are used to sustain the patient while a donor heart fortransplantation becomes available for the patient. There are also anumber of pacing devices used to treat CHF. However, in the chronicischemic heart, high rate pacing may lead to increased diastolicpressure, indicating calcium overload and damage of the muscle fibers.Finally, there are at least three surgical procedures for treatment ofheart failure: 1) heart transplant; 2) dynamic cardiomyoplasty; and 3)the Batista partial left ventriculectomy. Heart transplantation hasserious limitations including restricted availability of organs andadverse effects of immunosuppressive therapies required following hearttransplantation. Cardiomyoplasty includes wrapping the heart withskeletal muscle and electrically stimulating the muscle to contractsynchronously with the heart in order to help the pumping function ofthe heart. The Batista partial left ventriculectomy includes surgicallyremodeling the left ventricle by removing a segment of the muscularwall. This procedure reduces the diameter of the dilated heart, which inturn reduces the loading of the heart. However, this extremely invasiveprocedure reduces muscle mass of the heart.

One category of CHF is diastolic heart failure (DHF), which afflictsbetween 30% and 70% of those patients with heart failure. DHF is anepisodic clinical syndrome that can instigate pulmonary edema, possiblynecessitating hospitalization and ventilatory support. The heart is acomplex pump structured of two atria and two ventricles that pump bloodin parallel into the pulmonary circulation at a relatively low pressure(right ventricle peak systolic pressure is about 25 mmHg) and thesystemic circulation (left ventricle peak systolic pressure is about 120mmHg). During the diastolic phase of the cardiac cycle the ventricles ofthe heart fill via the respective atria. The pressure differential thatpropels blood from the respective venous circulations to the atria andventricles (systemic to the right ventricle and pulmonary to the leftventricle) is low, less than about 5 mmHg. On the left side, duringdiastole (when the mitral valve opens), pressure in the left atriumnormally is not more than 12 mmHg. Due to active diastolic relaxation atthe onset of diastole, the pressure difference between the left atriumand the left ventricle is augmented contributing to the early rapiddiastolic filling of the left ventricle. Diastolic pressures in theatrium and the ventricle at this phase of the cardiac cycle drop quicklyto less than 5 mmHg and equalize. At this point during diastole, theprocess of filling the left ventricle partially stops (diastiasis) andis renewed only towards late diastole, when active contraction of theatrium occurs, resulting in increased left atrial pressure and anincreased pressure differential between the atrium and the ventricle.Atrial contraction is very important for maintaining adequate leftventricular filling during exercise and other states of increasedcardiac output demand, or when the left ventricle fails to relaxnormally such as during ischemia or LV hypertrophy. Toward the end ofdiastole, pressure in the left ventricle (LVEDP) is increased but isnormally not more than 12 mmHg.

Disease states in which active and passive relaxation properties of theleft ventricle are disturbed, or the pumping and emptying capacity ofthe ventricle is reduced, may be translated to increased diastolicpressures in the left ventricle. The higher pressures and distension ofthe left ventricle cause a rise in wall stress and increased oxygenconsumption. Up to a limit, the increased diastolic pressure andincreased ventricular size result in augmented stroke volume. Thiscompensatory mechanism is limited and has a significant physiologicprice mainly when the slope of the pressure-volume curves turn steep,and left ventricular diastolic pressures becomes markedly high (>20mmHg). At this point, a state of pulmonary congestion may ensue, turninglater to a life threatening state of pulmonary edema.

A number of cardiovascular diseases can cause significant cardiacdysfunction and lead to the above-mentioned pathophysiologic state andpulmonary edema. These include: hypertension, ischemic heart diseasestate and post myocardial infarction, idiopathic dilated cardiomyopathy,valvular heart disease, including aortic stenosis, mitral stenosis,aortic regurgitation, mitral regurgitation, and combined valvular heartdisease. Other primary myocardial diseases such as post partum andhypertrophic cardiomyopathy may cause similar conditions. In all thesedisease states with either decreased ability for the left ventricle topump blood (systolic dysfunction) or reduced fling capacity (diastolicdysfunction) left ventricular diastolic pressure rises. Increaseddiastolic pressure in the left ventricle eventually in and of itselfbecomes a cause for greater degradation in cardiac function thanoccurred as a result of the original insult. The augmented pressures maycause as stated previously pulmonary congestion and dyspnea. At extremeconditions the clinical state may deteriorate to pulmonary edema.

There are several known techniques to attempt to overcome the state ofleft ventricular dysfunction, increased diastolic left ventricularpressures and pulmonary congestion. However, none are fullysatisfactory. For example, pharmacological treatments are the onlypractical methods for chronic therapy for most of the population withcongestive heart failure. The pharmacological agents used to treatcongestive heart failure result in a reduction in diastolic pressure andprevention of pulmonary and peripheral congestion discussed above, i.e.,diuretics, vasodilators and digoxin. Diuretics reduce the volume loadand thereby reduce preload and diastolic wall stress. Vasodilators havea dual effect in reducing arterial resistance as well as increasingvenous capacitance, thereby reducing preload and after load and wallstress throughout the cardiac cycle. These drugs, either direct actingon the vasculature or via neurohormonal mechanisms (ACE inhibitors), arelimited in their effect since they may cause hypotension in asignificant number of patients with myocardial dysfunction. Thesepharmacological agents are of limited value mainly because of their sideeffects. The use of diuretics is associated with side effects related tothe drugs and to the detrimental effect on renal function. Vasodilatorshave also many side effects some of which limit the use of the drugs andtheir efficacy including hypotension in many patients. Drug therapyresults in many of the patients in relative clinical stability. However,episodes where intraventricular diastolic pressure may rise abovephysiologic needs for cardiac stroke volume augmentation and culminateinto pulmonary edema occur often and are very difficult to manage.

In extreme acute situations, temporary assist devices and intraaorticballoons may be helpful. Cardiac transplantation and chronic LVADimplants are solutions available for a small part of the patientpopulation and as last resort. However, all the assist devices currentlyused are intended to improve pumping capacity of the heart and increasecardiac output to levels compatible with normal life. Finally, cardiactransplantation is another solution, but is not a very practical and islimited to extreme cases and as are the various assist devices. Themechanical devices were built to allow propulsion of significant amountof blood (liters/min) and this is also their main technologicallimitation. The need for power supply, relatively large pumps and dangerof hemolysis and infection are all of significant concern.

Thus, there exists a long-felt and as of yet unsolved need for atreatment that addresses the course of congestive heart failure, and inparticular the high pressure of the left ventricle and the compoundingfactors that are associated with it. It would therefore be desirable toprovide methods, apparatus and treatments that beneficially reduce andregulate the pressure within the left ventricle. It is an object of thepresent invention to provide methods and apparatus for reducing leftventricular end diastolic pressure, and more particularly to providemethods and apparatus without deleterious side effects. It is a furtherobject of the present invention to provide methods and apparatus thatcan be used in a minimally invasive manner for both acute and chronictreatments.

SUMMARY OF THE INVENTION

The present invention reduces the increased diastolic pressure that canoccur as part of the clinical syndrome referred to as Congestive HeartFailure (CHF). Passive and semi-passive devices to reduce leftventricular end-diastolic pressure are disclosed, and in preferredembodiments, a shunt-type device allows a small volume of blood to bereleased from the left ventricle to reduce the pressure. Certainembodiments use a passive check-valve that allows flow only above agiven threshold pressure, while others use a passive check-valve thatallows flow only within a window between a lower pressure threshold anda higher-pressure threshold. Embodiments employing check valves preventshunting during left ventricular systole. Alternatively, semi-passiveembodiments have a valve activated by an external signal, such as anintra-corporeal electrical battery or an externally coupled energysource. A third type of preferred embodiment of the invention employs andevice such as a pump to actively move blood, with the intent ofpreventing further deterioration of the patient's heart failure orallowing for some reversal of the heart failure. For example in patientspresenting with diastolic heart failure (DHF) the present inventionprevents this occurrence by reducing diastolic pressures in the leftatrium below the excessive levels that would otherwise have causedpulmonary edema.

The present invention is thus directed to methods and apparatus fordecreasing pressure in a first portion of a vessel of the cardiacstructure of a patient by implanting a shunt communicating with an areaoutside said first portion, whereby a volume of blood sufficient toreduce pressure in said first portion is released. Preferably, the firstportion comprises the left ventricle and the pressure reduced is the enddiastolic pressure, which is accomplished by having the shuntcommunicate with the left ventricle so a small volume of blood isreleased from the left ventricle to reduce the end diastolic pressure.Most preferably, the shunt selectively permits flow when a pressuredifferential between the left ventricle and another chamber of a heartabove a threshold pressure, whereby shunting is prevented during leftventricular systole, or, alternatively, selectively permits flow when apressure differential between the left ventricle and another chamber ofa heart is between a lower threshold and a higher threshold, wherebyshunting is again prevented during left ventricular systole. In certainembodiments a semi-passive check-valve is controlled and actuated by anexternal signal, either using a signal generated by an intra-corporealelectrical battery or an externally coupled energy source. In certainembodiments, the shunt has a pump with an input connected to the leftventricle, or other portion with excessive pressure, and an outputconnected to a volume of lower pressure. The preferred method ofimplanting the shunt to effect the present invention is by deploying atubular element having two ends and a tissue affixation element disposedat each of said ends via a catheter, preferably, the fixation element isa shape retaining metallic material that returns to its original shapeas part of the retention aspect of its function. In preferredembodiments of the apparatus, the tubular element is comprised of abiologically inert non-metallic material.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a perspective view of a first embodiment of an implantableshunt made in accordance with the present invention;

FIG. 2 is a side elevation view, in cross-section as shown by lines 2-2in FIG. 1, illustrating the placement of the shunt shown in FIG. 1 in aseptum, and showing diagrammatically the use of a pump to augment flowin certain embodiments; and

FIGS. 3-5 are a cross sectional view of a patient receiving a shunt madein accordance with the present invention via percutaneous placement.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS

Referring now to FIG. 1, there is shown a perspective view of a firstembodiment of a shunt 100 made in accordance with the present invention.The shunt 100 is comprised of a fixation element 110, which is shown asa planar circular element. It will be understood, however, that thefixation element 110 can be circular, polygonal, spiral or many othershapes. Moreover, the fixation element can lie in a single plane or becurved in multiple planes, such as in a helical configuration. It can beconstructed of a variety of materials that offer the elastic range andspring-like characteristics that will enable passage through a catheterlumen, or through the lumen of another implantation assistance device,in a relatively straightened configuration and then recovery of its fillfixation configuration shape. In certain embodiments, the fixationelement can be made of reduced size and then expanded through the use ofshape-memory alloys (SMA's), such as nickel-titanium (NiTi, also knownas nitinol), that change shape in response to temperature changes andwhich are fabricated such that the temperature change from below bodytemperature to body temperature causes the shape conversion necessaryfor implantation. If SMA materials are not used, suitable materialsinclude super-elastic metals, such as NiTi or stainless steel, such asthe alloy ELGILOY®, commonly used for medical implants. Additionally,polymeric materials can be used to form the fixation element or as acoating over a metallic core. The fixation element may be coated and/ortextured as so as to increase its biocompatibility or to increase thedegree to which it quickly becomes endothelialized, which may be desiredin some implantation conditions.

As illustrated, the fixation element 110 surrounds and positions theshunt tube element 120, which is provided so as to enable passage ofblood from a region of high pressure, such as the left atrium, to aregion of lower pressure, such as the right atrium. The dimensions ofthe shunt tube element 120 are chosen so as to be as small as possiblewhile still allowing sufficiently rapid fluid flow without endangeringblood coagulation induced by blood stasis or low-flow zones.Computational fluid dynamics methods can be used to appropriately shapethe element so as to minimize low-flow zones and maximize laminar flow.The inside diameter of the shunt tube is preferably greater than 1 mmand less than 5 mm, but it will be understood that a wide range ofshapes and diameters can be constructed that will effect the purpose ofthe present invention in a variety of patients and flow conditionswithin those patients. The shunt tube element 120 is preferably formedof either metallic or polymeric materials and may be coated and/ortextured as mentioned above. Pyrolitic carbon coating, as is commonlyused in implantable mechanical heart valves, can be used to increase thedegree to which the surface is biologically inert. Examples of suchcommercially available materials include On-X{circle over (R)} Carbon,from Medical Carbon Research Institute, LLC, of Austin, Tex.

Also illustrated in FIG. 1 is a valve element 130, which as explainedbelow is not necessarily included in all embodiments within the scope ofthe present invention and can be of a variety of forms. As illustrated aleaflet 131,132 can be used, either in a single piece or as a dualleaflet design as illustrated. In the embodiment shown in FIG. 1, eachleaflet 131,132 is a flat plate that pivots to open and close theorifice of the shunt tube. A ball-and-socket design can be used as well.Another alternative design is the duckbill-type valve. The valve elementcan be formed using the same range or materials and coatings mentionedabove for the shunt tube.

From the foregoing, it will be appreciated by those of skill in the artthat the present invention is well adapted to percutaneous placement viafemoral access, however, other implantation techniques such as surgicaltechniques using either an open chest procedure or those using minimallyinvasive techniques are also within the scope of the present invention.

The concepts of allowing pressure to be relieved in one area of thecirculation by shunting to an area of lower pressure as disclosed hereinmay take many embodiments, all of which will be apparent to those ofskill in the art upon review of the foregoing descriptions of thephysiology and medicine involved, and the description of the embodimentof FIG. 1.

In accordance with the present invention, the device may or may notinclude the valve element 130, since in certain patients or to treatcertain conditions a valve would add complexity while not providingnecessary functionality. Similarly, depending upon the circumstances ofuse, the valve element 130 may be either passive (actuated by the forceof blood) or active (actuated by some other portion of the device). Inactive valve embodiments, the valve element 130 may include electric orelectromagnetic elements that can be selectively actuated to open andclose the valve element 130 or, if the valve element is designed forgradual opening and closing, move the valve element 130 between a firstposition and a second position. In some embodiments, the valve will bechosen and designed so that it responds only upon certain conditionsoccurring within the heart, such as the following: absolute left atrialpressure, differential atrial pressure, other intra-cardiac pressures,other cardiovascular pressures, or other physiological conditions thatmight correlate to an exacerbated state of diastolic heart failure, suchas blood oxygen saturation or pH. In such embodiments, response to anygiven pressure or differential pressure will imply that a portion of theimplanted device is in fluid communication with the relevant pressuresource or sources. These embodiments will provide robust and reliablefunctionality by being mechanical and operating with signal inputs. Allshunts, whether they include a valve or not can be further enhanced byincluding a check-valve that will prevent backflow. Those of skill inthe art will appreciate that it is typically desirable to prevent flowfrom the right heart to the left heart, and thus one or more checkvalves can be appropriately placed. A double-check valve allows bloodpressure above a lower limit but below a higher limit to actuate thevalve, thus in a preferred embodiment, shunting blood from the left sideto the right side only during a period of diastole.

Referring now to FIG. 2, another aspect of the devices of the presentinvention is that the shunt 100 may or may not be in fluid communicationwith a pump 140, such as either a surgically implanted pump thatcontinuously moves a small amount of blood from one chamber or area toanother, for example from the left ventricle chamber to the aorta forchronic reduction of LVEDP. Alternatively, the invention can include acatheter-based pump that continuously moves a small amount of blood fromthe LV chamber to the aorta for acute reduction of LVEDP. In certainpreferred embodiments, the pump and valve will have a heart-synchronizedactuated valve to allow specific regimens of left-to-right shunting tobe applied. As seen in FIG. 2, after the shunt 100 is placed in a septumor other area, the pump 140 may be placed so as to direct fluid towardthe shunt, the pump may be directly connected to the shunt, juxtaposedto the shunt, or displaced from the shunt but capable of directing flowin such a way as to effect more efficient pressure reduction.

FIG. 2 shows an implant similar to that of FIG. 1 that is placedsurgically for the chronic reduction of LVEDP. This device includes arelatively small-sized pump 140, which can be similar to those used inLeft-Ventricular Assist Devices (LVADs). Unlike the LVAD, however, thedisclosed invention does not seek to significantly “support” thefunction of the left ventricle by pumping blood from the LV chamber tothe body. Rather, it is intended only to “offload” the excessivepressure that builds through the diastolic phase of the cardiac cycle insome CBF patients. Whereas a normal LVEDP is in the range of 6-12 mmHg,patients with diastolic dysfunction heart failure (DDHF), end-diastolicpressure (EDP) in the left atrium (LA) and left ventricle (LV) can riseconsiderably above normal levels. Therefore the present inventionencompasses a number of embodiments that are both capable of beingeither implanted during a surgical procedure or using a catheter(percutaneous). The shunt 100 allows blood to flow in the directionshown by the arrows so long as there is a lower pressure in the chamberor vessel adjoining the LV. In any embodiment, the methods and apparatusof the present invention reduce EDP, and in particular mitigate the mostsevere consequences of significantly increased EDP, such as pulmonaryedema.

Thus, in preferred embodiments of the present invention the shunt isdisposed in a wall between the chambers of a patient's heart, and mostpreferably, disposed in the atrial septum to permit blood to flow fromthe left ventricle when the pressure within the ventricle exceeds thepressure of the adjoining atrial chamber. In another particularembodiment, a sophisticated shunt apparatus implanted in theintra-atrial septum to allow intermittent and controlled blood flow fromthe left atrium to the right atrium (RA), thereby reducing LAEDP.Alternatively, the shunt might have its origin in locations other thanthe LA, such as the LV, and might have its output at locations otherthan the RA, such as the light ventricle (RV).

As explained above, although one class of embodiments of the presentinvention is designed to be purely mechanical and will have certainadvantages, the present invention also encompasses additionalembodiments wherein additional features such as internal signalprocessing unit 148 and an energy source 150, such as a battery, areincluded. In such embodiments, the shunts described above will include avalve apparatus that responds to conditions other than those occurringwithin the heart and/or has internal signal processing requiring anenergy source. A device of this type responds according to programmedalgorithms to all of the conditions mentioned above. The signalprocessing ability of devices in such embodiments enable adaptiveapproaches as well, in which the device response to conditions willchange over time according to a pre-programmed adaptation algorithm.Such embodiments will include additional apparatus, such as a powersource 150, sensors 155 and the like. The provision of implantable,programmable electrical devices that collect cardiac data and effect theoperation of certain other elements of a device are well known in thefield of cardiac pacing, for one example. In one particular embodiment,the actively controlled valve of the shunt as in senses and responds toelectrical signals so as to act in synchronization with the cardiaccycle.

Either passive or active devices may be linked to an external indicator157, such as pendant worn by the patient, that displays the devicestatus. Such an indicator enables the patient to notify a physician inthe event of an activation of the implanted device that corresponds tothe significantly exacerbated state heart failure. In this case, thedevice will be acting to prevent the occurrence of pulmonary edemaduring the time that the patient notifies a physician and then undergoesmedical treatment to reduce the severity of the patient's condition.

Similarly, any embodiment of the present invention may be designed sothat an external device can be used on occasion to either mechanicallyadjust (in the case of passive devices; for example, by magneticcoupling) and/or to reprogram (in the case of active devices) thefunctioning of the implanted device.

The methods mentioned above will prevent from excessive pressures tobuild up in the left ventricle and help restore wall stress in diastoleand systole to normal values quickly thus helping the introduction ofpharmacological agents as adjunct therapy or vice versa. This mode oftherapy will be complementary to the current management of the patientsand allow more controlled stabilization. It can be added as a componentof cardiac pacemaker (dual or biventricular) and derive the power supplyfrom the pacemaker battery.

The pressure/flow/volume requirements of the various embodiments of thepresent invention will be determined using methodologies similar tothose used to design a Left Ventricular Assist Device (LVAD) but withcertain distinctly different flow requirements, rather than the intentof supporting systemic circulation requirements found in a LVAD. Thus,certain shunts made in accordance with the present invention can usedesigns and dimensions that would not be appropriate or adequate for anLVAD. Patients with heart failure dominated by systolic dysfunctionexhibit contraction abnormalities, whereas those in diastolicdysfunction exhibit relaxation abnormalities. In most patients there isa mixed pathophysiology. Normal pulmonary venous pressure (PVP)necessary for the normal LV to adequately fill and pump is less than 12mmHg. Patients with systolic dysfunction have larger LV volume tomaintain SV and may need increased PVP to fill (mixed systolic diastolicdysfunction). Patients with diastolic dysfunction need increased PVP forthe LV to fill and adequately pump.

The hemodynamic performance of the present invention, and thus thedesign of the shunt and its actuation, placement etc. will be determinedby a variety of factors, for example, the following table is in the formof:

IF ({LAEDP} AND/OR {Mean LA P}) AND/OR ({ΔLAEDP-RAEDP} AND/OR {ΔMean LAP-Mean RA P}) THEN {ACTION}

In which LAEDP, Mean LA P, RAEDP and Mean RA P refer to minima, maximaor ranges for the respective pressures (please specify which in thetable), and the AND/OR indicate that a logical operator or an NA (notapplicable) should be entered

IF AND/ Mean AND/ Δ Atrial AND/ Δ mean Then Scenario LAEDP OR LA P OREDP OR atrial P (Action) Ex. Exceeds Or Exceeds NA NA NA NA Removesufficient 25 20 blood from the LA to reduce LA pressure by 5 mmHg

Thus for example, a chronic device can be a preventive device where whenpressures rise for some reason to dangerous levels the pump goes intoaction and helps to lower the pressure in the left ventricle, therebypreventing the acute development of dyspnea and pulmonary edema andassures that the LVDP are always at an optimal level of no more than 15mmHg.

In other embodiments and for other indications, the present inventionmight move an extra volume of blood from the LV into the aorta. To doso, the pump 140 must be capable of moving blood from a chamberexhibiting 20 mmHg in diastole to 70 mmHg in the aorta. Another possiblechamber where blood from the LA (throughout the cardiac cycle) or LV(only in diastole) can be directed to is the Right Atrium, andalternatively right ventricle. The benefit of directing blood from LA toRA is that the pressure differences are smaller and the blood can bemoved in diastole and systole as well. Filling of the atria (R and L)during the systolic phase of the cardiac cycle determines the pressurein the atria at the onset of diastole and the opening of the valves.

Those of skill in the art will appreciate that there are a number oftechniques for placement and locations for placement of shunts made inaccordance with the present invention. For example, a surgicallyimplanted passive shunt can be placed between the left ventricle and theright atrium for chronic reduction of LVEDP. Alternatively, a surgicallyimplanted passive shunt can be placed between the left atrium and theright atrium for chronic reduction of LVEDP. For percutaneous placement,a catheter-based passive shunt can be inserted from the right atriumtrans-septally into the left atrium for acute reduction of LVEDP.Another catheter-delivered embodiment is a passive shunt that isimplanted from the right atrium trans-septally into the left atrium forchronic reduction of LVEDP.

Although the present invention provides new and useful methods oftreatment, the techniques of implanting shunts as described herein iswell known. For one example, in a preferred embodiment of the presentinvention, as illustrated in FIGS. 3-5, a transseptal needle set 160 isadvanced toward the wall of the right atrial septum. Access has beenmade from the femoral vein with the system being advanced through theinferior vena cava and into the right atrium. Devices that allow suchaccess and subsequent transseptal puncture are available from CookIncorporated. For example, the procedure can be carried out using astainless steel and obrturator set TSNC-18-71.0 for adults andTSNC-19-56.0 for pediatric patients. Once transseptal puncture has beenachieved, a guidewire 170 is exchanged for the needle component in thecommercially available device described above and then passed into theleft atrium. The process of securing catheter access to the left atriumby way of a transseptal puncture is further described in the standardmedical text Braunwald, Heart Disease, (Ch. 6, p. 186) which isincorporated herein by reference. After the transseptal sheath 165 ispositioned in the left atrium, as described above, the placement of ashunt 100 made in accordance with the present invention is initiated.The following is a generalized sequence; the placement procedure will bedone according to the typical methods of interventional cardiology asare well known to physicians trained in that subspecialty. The typicalsupporting apparatus found in the cardiac catheterization laboratorywill be used, such as fluoroscopy for visualization and hemodynamic andECG monitoring equipment to assess catheter position and patient vitalsigns.

The dilator and wire will be withdrawn from the sheath that now extendsfrom the femoral vein access point in the patient's groin to the leftatrium, traversing the femoral vein, the illiac vein, the inferior venacava, the right atrium, and the atrial septum The delivery catheter willbe passed through the sheath while under fluoroscopic visualization.Radiopaque markers are provided on this catheter as well as the sheathin order to locate specific points. The delivery catheter is carefullyand slowly advanced so that the most distal portion of the left-atrialfixation wire is emitted from the distal opening of the catheter andinto the chamber of the left atrium. The fixation wire is formed from aspring-like material and/or may be super-elastic of shape-memory alloy,so that as it leaves the constraint provided by the inner lumen of thedelivery catheter, it reforms into its fully formed shape, which maycircular or polygonal as previously disclosed. The assembly of thesheath and the delivery catheter are then slowly retracted en bloc so asto withdraw the fixation wire towards the atrial septum. The physicianstops this retraction when it becomes apparent by fluoroscopicvisualization as well as by tactile feedback that the fixation wire hasbecome seated against the atrial septum. At that point, the sheath aloneis retracted, uncovering the shunt and positioning it within the openingthat has been created within the atrial septum. The sheath is thenfurther retracted, allowing the right-atrial fixation wire to reforminto its fully formed shape. The entire shunt assembly is then detachedfrom the delivery catheter system The shunt is controlled within thedelivery catheter by means of long controller wire that has independenttranslational control within the catheter lumen. This attachment isformed by any conventional method, e.g., a solder or adhesive or thelike that will mechanically detach at a prescribed tension level, thatlevel being exceeded by the physician at this point in the procedure byfirmly retracting the controller wire.

Although certain embodiments have been set forth and described herein,numerous alterations, modifications, and adaptations of the conceptspresented will be immediately apparent to those of skill in the art, andaccordingly will lie within the scope of the present invention, asdefined by the claims appended hereto.

1. A device for decreasing blood pressure in the left atrium of a heartof a human with congestive heart failure, the device comprising: a shunttube element configured for percutaneous placement across an atrialseptum of the human with congestive heart failure so as to define apassageway between the right atrium and the left atrium through theatrial septum; a valve element disposed within the shunt tube elementand configured to open to permit blood to flow from the left atrium tothe right atrium through the shunt tube element only when the bloodpressure in the left atrium exceeds the blood pressure in the rightatrium; and a fixation element comprising first and secondself-expanding end regions configured to retain the shunt tube elementwithin the atrial septum, the device being configured such that thefirst self-expanding end region communicates with the left atrium andthe second self-expanding end region communicates with the right atriumand reduces the blood pressure in the left atrium by transferring bloodfrom the left atrium to the right atrium through the shunt tube elementresponsive to a predetermined differential atrial pressure.
 2. Thedevice of claim 1, wherein the first and second self-expanding endregions of the fixation element comprise first and second flanges. 3.The device of claim 2, wherein the first and second flanges are annular.4. The device of claim 2, wherein the first and second flanges areconfigured to respectively engage first and second sides of the atrialseptum.
 5. The device of claim 1, wherein the valve element comprises atleast two leaflets.
 6. The device of claim 1, wherein the shunt tubeelement is cylindrical.
 7. The device of claim 1, wherein the valvecomprises a passive check-valve that allows blood flow only above agiven threshold pressure.
 8. The device of claim 1, wherein the fixationelement surrounds and positions the shunt tube element.
 9. The device ofclaim 1, wherein the valve element comprises a plurality of leaflets.10. The device of claim 1, wherein the valve element comprises aleaflet.